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pubmed-article:11248418pubmed:abstractTextPhotodynamic therapy (PDT) activates the mitochondrial pathway of apoptosis, for which the release of cytochrome c into the cytosol is considered critical. To further elucidate the role of cytochrome c release in PDT-induced apoptosis, we monitored cytochrome c localization immunocytochemically and related it to nuclear apoptosis of the same cells. When mouse L5178Y-R cells were treated with 300 nM phthalocyanine (Pc) 4 and 0-75 mJ/cm(2) red light, cytochrome c release had a dose response similar to that of clonogenic cell killing, with nearly identical threshold doses. Within individual cells, the release of cytochrome c appeared to be an all-or-none phenomenon. Moreover, it was tightly associated with activation of a caspase-3-like protease and changes in nuclear morphology. Thus, in response to Pc 4-PDT, the release of cytochrome c from mitochondria is a key determinant of apoptotic cell death.lld:pubmed
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pubmed-article:11248418pubmed:articleTitlePhthalocyanine 4 photodynamic therapy-induced apoptosis of mouse L5178Y-R cells results from a delayed but extensive release of cytochrome c from mitochondria.lld:pubmed
pubmed-article:11248418pubmed:affiliationDepartment of Radiation Oncology, Case Western Reserve University School of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106-4942, USA.lld:pubmed
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pubmed-article:11248418pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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